Related Experiment Video

Updated: May 30, 2026

Knockdown of FAM83A to Verify Its Role in Cervical Cancer Cell Growth and Cisplatin Sensitivity
04:20

Knockdown of FAM83A to Verify Its Role in Cervical Cancer Cell Growth and Cisplatin Sensitivity

Published on: February 9, 2024

Knockdown of survivin (BIRC5) causes apoptosis in neuroblastoma via mitotic catastrophe

Fieke Lamers1, Ida van der Ploeg, Linda Schild

  • 1Department of Oncogenomics, Academic Medical Center, University of Amsterdam, Meibergdreef 15, PO Box 22700, 1105 AZ Amsterdam, The Netherlands.

Endocrine-Related Cancer
|August 24, 2011
PubMed

Insights

Survivin (BIRC5) is upregulated in neuroblastoma, promoting cancer cell survival by stabilizing microtubules. Silencing BIRC5 triggers apoptosis via mitotic catastrophe, making it a promising therapeutic target for neuroblastoma.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Neuroblastoma often involves gain of chromosome 17q.
  • BIRC5 (Survivin) is a key protein in apoptosis and microtubule stabilization.
  • Overexpression of BIRC5 is implicated in various cancers.

Purpose of the Study:

  • To investigate the role of BIRC5 in neuroblastoma.
  • To determine the mechanism by which BIRC5 promotes neuroblastoma survival.
  • To evaluate BIRC5 as a therapeutic target in neuroblastoma.

Main Methods:

  • Analysis of Affymetrix mRNA expression data.
  • Silencing of BIRC5 using antisense molecules in neuroblastoma cell lines.
  • Assessment of apoptosis via PARP cleavage and FACS analysis.
  • Immunofluorescence microscopy to analyze cellular morphology.
  • Investigation of the involvement of P53 and CASP2 pathways.

Main Results:

  • BIRC5 is significantly upregulated in neuroblastoma compared to normal tissues.
  • High BIRC5 expression correlates with unfavorable prognosis, independent of 17q gain.
  • BIRC5 silencing induced massive apoptosis in neuroblastoma cells.
  • BIRC5 silencing led to multinucleated cells, indicating mitotic catastrophe.
  • Apoptosis was mediated by P53 activation and CASP2, and could be rescued by CASP2 inhibition.

Conclusions:

  • BIRC5 stabilizes microtubules within the chromosomal passenger complex in neuroblastoma.
  • The anti-apoptotic role of BIRC5 in neuroblastoma is linked to mitotic catastrophe.
  • BIRC5 is a potential therapeutic target for neuroblastoma treatment.

More Related Videos

Detection of Mitochondria Membrane Potential to Study CLIC4 Knockdown-induced HN4 Cell Apoptosis In Vitro13:20

Detection of Mitochondria Membrane Potential to Study CLIC4 Knockdown-induced HN4 Cell Apoptosis In Vitro

Published on: July 17, 2018

Related Concept Videos

The Intrinsic Apoptotic Pathway01:31

The Intrinsic Apoptotic Pathway

Internal cellular stress, such as cellular injury or hypoxia, triggers intrinsic apoptosis. The B-cell lymphoma 2 (Bcl-2) family of proteins are the primary regulators of the intrinsic apoptotic pathway. For example, during DNA damage, checkpoint proteins, such as Ataxia Telangiectasia Mutated (ATM protein) and Checkpoints Factor-2 (Chk2) proteins, are activated. These proteins phosphorylate p53 which further activates pro-apoptotic proteins, such as Bax, Bak, PUMA, and Noxa, and inhibits...
The Retinoblastoma Gene01:20

The Retinoblastoma Gene

Tumor suppressor genes are normal genes that can slow down cell division, repair DNA mistakes, or program the cells for apoptosis in case of irreparable damage. Hence, they play an essential role in preventing the proliferation of damaged cells.
The first-ever tumor suppressor gene called Rb was identified in retinoblastoma - a rare eye tumor in children. In inherited forms of the disease, a child inherits one defective copy of the Rb gene, which predisposes them to retinoblastoma. However,...
The Extrinsic Apoptotic Pathway01:17

The Extrinsic Apoptotic Pathway

The extrinsic apoptotic pathway is initiated when extracellular death-inducing signals, such as specific cytokines, activate the death receptors expressed on the cell surface. The immune cells involved in this pathway are natural killer cells (NK cells) and cytotoxic T-lymphocytes. NK cells are critical in innate immune response, while cytotoxic T-lymphocytes are associated with adaptive immune response. These cells recognize specific receptors expressed on the altered cells and activate...
Cellular Injury V: Apoptosis and Autophagy01:22

Cellular Injury V: Apoptosis and Autophagy

Cells respond to damage and stress through highly coordinated processes that decide whether they survive or undergo controlled self-destruction. Two major pathways involved in this regulation are apoptosis, a type of programmed cell death, and autophagy, a survival mechanism that helps cells adapt to adverse conditions.ApoptosisApoptosis removes aged or injured cells to maintain tissue balance. During this process, the cell shrinks, chromatin condenses and fragments, and membrane-bound...
Abnormal Proliferation02:23

Abnormal Proliferation

Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the daughter...
Apoptosis01:30

Apoptosis

Apoptosis is a combination of two Greek words, 'apo' and 'ptosis,' meaning separation and falling off, respectively. Hippocrates used this word to describe gangrene, which was caused due to bandaging of fractured bones. Apoptosis was distinguished from necrosis in 1970 when John Kerr reported observations of morphological changes occurring during apoptosis. During one experiment, he observed that the disruption of blood supply to the liver tissue resulted in a size reduction of the tissue.